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Year 5 notes > Neuro > Flashcards

Neuro Flashcards

1
Q

visual field defect in parietal lobe lesions

A

inferior homonymous quadrantanopia

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2
Q

visual field defect in occipital lobe lesiosn

A

homonymous hemianopia

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3
Q

location of lesion in Broca’s aphasia

A

frontal lobe (BF)

= expressive (BE) - speech is non-fluent and laboured

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4
Q

location of lesion in Wernicke’s aphasia

A

temporal lobe (TW)

= speech remains fluent but there are word substitutions and neologisms

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5
Q

midline cerebellum lesions cause

A

gait and truncal ataxia

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6
Q

cerebellum hemisphere lesions cause

A
  • intention tremor
  • past pointing
  • dysdiadokinesis
  • nystagmus
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7
Q

analgesia to avoid in migraine

A

opiates (give ibuprofen etc)

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8
Q

what to give in prophylaxis of migraine

A

propranolol (CI in asthma)

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9
Q

what to give in acute migraine

A

triptans (CI if CV disease/cerebrovascular disease)

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10
Q

prophylaxis of tension headache

A

low dose amitriptyline

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11
Q

treatment of acute cluster headache

A

nasal/SC triptans + high flow oxygen

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12
Q

prophylaxis of cluster headache

A

verapamil (2nd line = prednisolone + lithium)

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13
Q

why can trigeminal neuralgia cause ptosis

A

CNV compression i.e. by superior cerebellar artery

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14
Q

management of trigeminal neuralgia

A

carbamazepine - titrate upwards every 2 weeks until pain relieved

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15
Q

red flags for referral in trigeminal neuralgia

A
  • <40 years
  • pain only in ophthalmic division/bilaterally
  • sensory changes
  • deafness
  • history of skin/oral lesions
  • optic neuritis
  • family history of MS
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16
Q

LP findings in SAH

A

xanthochromia
increased opening pressure
increased protein

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17
Q

medication which can be given in SAH

A

nimlodipine (to prevent vasospasm)

3L normal saline fluids (give lots of sodium)

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18
Q

first line surgery for SAH

A

endovascular coiling

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19
Q

major RF of intracerebral haemorrhage

A

HTN

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20
Q

treatment of intracerebral haemorrhage

A

reverse anticoagulation

don’t give aspirin

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21
Q

what to do if an ischaemic stroke is inappropriate for thrombectomy

A

CT angiogram

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22
Q

how to diagnose carotid/vertebral artery dissection

A

MRA/CTA

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23
Q

symptoms of pituitary apoplexy

A

headhace
visual deficits
ophthalmoplegia
altered GCS

due to pituitary gland enlarging

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24
Q

management of idiopathic intracranial HTN

A
  • weight loss
  • diuretics i.e. ACETAZOLAMIDE
  • topiramate
  • repeat LP
  • surgery? optic nerve sheath decompression
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25
Q

what might a CT venogram show in venous sinus thrombosis

A

absence of sinus
‘hyperdensity’
‘empty delta sign’ (filling defect)

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26
Q

features of Meniere’s

A

vertigo
fluctuating tinnitus
deafness
fullness in one ear 9

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27
Q

type of nystagmus in BPPV if superior semicircular canal is involved

A

rotatory nystagmus

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28
Q

type of nystagmus in BPPV if lateral semicircular canal is involved

A

horizontal nystagmus

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29
Q

clinical presentation of lesion in cerebellar hemisphere

A

limb ataxia IPSILATERAL to lesion

tendency to fall towards affected side + nystagmus + dysarthria

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30
Q

clinical presentation of lesion in midline vermis of cerebellum

A

truncal ataxia

difficulty sitting/standing (gait ataxia)

typically without classic triad of limb ataxia + dysarthria + nystagmus

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31
Q

clinical presentation of lesion in flocuclonodular lobe of cerebellum

A

truncal ataxia
vertigo (damage to vestibular reflex pathways)
vomiting
nystagmus

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32
Q

why do cerebellar lesions at midline sites result in headache and vomiting

A

early obstruction of cerebral aqueduct in midbrain/4th ventricle = hydrocephalus with dilated 3rd and lateral ventricles = headache, vomiting and eventually papilloedema

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33
Q

MAVIS (causes of ataxia)

A
  • MS
  • Alcohol
  • Vascular (stroke)
  • Inherited (Friedrich’s, spinocerebellar ataxia, ataxia telangiectasia)
  • SOL
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34
Q

generalised seizures

A
  • absence (can be caused by hyperventilation)
  • tonic-clonic
  • myoclonic
  • atopic (often combined with a myoclonic jerk followed by transient loss of muscle tone)
  • tonic (generalised increased tone)
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35
Q

focal seizures are?

A

either frontal, temporal, occipital, parietal

may have aura, LOC, decreased consciousness, tonic-clonic

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36
Q

what type of seizure is Jacksonian March

A

frontal seizure

seizure spreads from the distal part of the limb towards the ipsilateral face (clonic movements travelling proximally)

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37
Q

HEAD (signs of temporal seizures)

A
  • Hallucinations (auditory/sensory)
  • Epigastric sensation/emotional
  • Automatisms (lip smacking, pulling at clothing)
  • Deja-vu/dysphasia post octal
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38
Q

features of occipital seizure

A
  • positive or negative visual phenomena

- flashing lights, spots or simple patterns

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39
Q

features of parietal seizure

A
  • somatosensory (tingling, shock sensation, pain)
  • contralateral altered sensation
  • distorted body image
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40
Q

what is Todd’s paresis

A

focal weakness in a part of the body after seizure - localising to one side - subsides completely within 48hours

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41
Q

drugs for tonic-clonic or atonic seizures

A
  • sodium valproate

- lamotrigine/CBZ

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42
Q

drugs for focal seizures

A
  • lamotrigine/CBZ

- sodium valproate/levetiracetam

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43
Q

drugs for absence seizures

A
  • ethosuximide/sodium valproate

NOT CBZ (exacerbates)

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44
Q

drugs for myoclonic seizures

A
  • sodium valproate
  • leviteracetam

NOT CBZ (exacerbates)

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45
Q

side effects of carbamazepine

A

agranulocytosis
aplastic anaemia
teratogenic in first trimester

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46
Q

which anti-epileptics are P450 inhibitors

A

sodium valproate

therefore can increase effects of other AEDs

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47
Q

which anti-epileptics are P450 inducers

A

carbamazepine

phenytoin

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48
Q

side effects of lamotrigine

A

Steven Johnson’s
leukopenia
nausea, tremor, vomiting

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49
Q

side effects of phenytoin (PHENYTOIN)

A
  • P450 interactions (inducer)
  • hirsutism
  • enlarged gums (gingival hyperplasia)
  • nystagmus
  • yellow-browning of skin
  • teratogenicity
  • osteomalacia
  • interference with folate metabolism
  • neuropathies (vertigo, ataxia, headache)
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50
Q

effects of phenytoin overdose

A 
nystagmus
diplopia
slurred speech
ataxia
confusion
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51
Q

driving after 1st unprovoked seizure

A

6 months

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52
Q

driving after LOC/LOA with no clinical pointers

A

6 months

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53
Q

driving after >2 LOA without reliable prodrome

A

12 months

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54
Q

driving after epilepsy

A

12 months

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55
Q

driving after epilepsy - AED withdrawal

A

until 6 months post cessation

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56
Q

what is motor neurone disease

A

progressive degeneration of motor neurones in the motor cortex + in the anterior horns of the spinal cord

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57
Q

4 types of MND

A
  • progressive muscular atrophy
  • primary lateral sclerosis
  • progressive bulbar palsy
  • amyotrophic lateral sclerosis
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58
Q

features of ALS

A
  • 6 months progressive weakness of a limb e.g. foot drop
  • onset is focal, distal, asymmetrical and progresses segmentally form one limb to another
  • sphincters and eyes NOT affected
  • UMN + LMN features
  • 30% bulbar onset - speech or swallowing impairment (bilateral, asymmetrical tongue wasting)
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59
Q

type of dementia associated with ALS

A

fronto-temporal dementia

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60
Q

which drug can you use in ALS (doesn’t do much)

A

riluzole

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61
Q

features of progressive muscle atrophy

A
  • LMN signs - wasting, weakness and fasciculation, but tendon reflexes often preserved
  • begins asymmetrically in small muscles of hands or feed and spread
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62
Q

features of primary lateral sclerosis

A
  • UMN lesions - initially in legs before progressing to arms
  • diagnosis of exclusion + signs remained solely UMN for 3+ years
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63
Q

causes of progressive bulbar palsy

A
  • MND
  • stroke
  • MG
  • central pontine myelinolysis
  • GBS
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64
Q

features of pseudo bulbar palsy

A
  • bilateral UMN lesions
  • spastic tongue, brisk jaw jerk
  • emotional incontinence
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65
Q

causes of pseudo bulbar palsy

A
  • MS
  • MND
  • stroke
  • CPM
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66
Q

nerve roots of radial, median and ulnar nerves

A
  • radial = C5-T1 (anatomical snuffbox)
  • median = C6-T1 (lateral 3.5 digits)
  • ulnar = C7-T1 (medial 1.5 digits)
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67
Q

motor and sensory features median nerve problem

A
  • motor = thenar wasting

- sensory = radial 3.5 fingers and palm, pain in hand, Tinel’s and Phalen’s positive

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68
Q

motor and sensory features of ulnar nerve problem

A
  • motor = partial claw hand, hypothenar wasting, weakness and wasting of 1st dorsal interosseous
  • sensory = ulnar 1.5 fingers
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69
Q

motor features of radial nerve problems

A
  • low = finger drop
  • high = wrist drop
  • v high = triceps paralysis, wrist drop
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70
Q

motor and sensory features of high brachial plexus problem (C5-6)

A

Erb’s palsy (waiter’s tip)

C5-6 dermatome

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71
Q

motor and sensory features of low brachial plexus problem (C8-T1)

A

Klumpke’s (claw hand)

C8-T1 dermatome

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72
Q

motor and sensory features of sciatic nerve injury (L4-S3)

A
  • motor = hamstrings, all muscles below know

- sensory = below knee laterally and foot

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73
Q

motor and sensory features of common peroneal nerve injury (L4-S1)

A
  • motor = foot drop, weak ankle dorsiflexion and eversion - INVERSION INTACT
  • sensory = below knee laterally
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74
Q

motor and sensory features of tibial nerve injury (L4-S3)

A
  • motor = can’t plantar flex (can’t stand on tiptoe), weak foot inversion and weak toe flexion
  • sensory = sole of foot
75
Q

causes of predominantly MOTOR loss peripheral neuropathy

A
  • Guillain-Barre
  • porphyria
  • lead poisoning
  • Charcot-Marie-Tooth
  • CIDP
  • diphtheria
  • inclusion body myositis
  • myotonic dystrophy
76
Q

causes of predominantly SENSORY loss peripheral neuropathy (ABCDE)

A
  • alcoholism, amyloidosis
  • B12 deficiency
  • carcinoma, CMT
  • diabetes, drugs i.e. isoniazid (causes B6 deficiency)
  • every vasculitis

uraemia, leprosy

77
Q

causes of dysphonia (reduction in sound/volume)

A
  • laryngitis
  • CNX lesion
  • Parkinson’s
78
Q

what is non-fluent aphasia with comprehension intact

A

Broca’s aphasia (expressive)

79
Q

what is non-fluent aphasia with comprehension impaired

A

global aphasia

80
Q

what is fluent aphasia with comprehension intact

A

conduction aphasia

81
Q

what is fluent aphasia with comprehension impaired

A

wernicke’s aphasia - receptive (word salad)

82
Q

cause of wernicke’s aphasia

A

lesion of superior temporal gyrus - supplied by inferior division of left MCA

83
Q

cause of Broca’s aphasia

A

lesion of inferior frontal gyrus - supplied by superior division of left MCA

84
Q

cause of conduction aphasia

A

stroke affecting arcuate fasiculus Connection between wernicke’s and Broca’s area)

85
Q

cause of global aphasia

A

large lesion affecting Broca’s, wernicke’s and arcuate fasicuclus

86
Q

types of tremor

A
  • physiological (hyperthyroid)
  • rest (Parkinsonism)
  • postural (absent at rest, present in maintained posture)
  • flapping
  • intention (cerebellar)
  • holms or rubral tremor = resting + action
87
Q

examples of postural tremor

A
  • benign essential tremor (improves with alcohol)
  • thyrotoxicosis
  • anxiety
  • beta-agonists
88
Q

features of multiple system atrophy

A
  • severe early AUTONOMIC dysfunction - postural BP drop, erectile dysfunction, atonic bladder
  • Parkinsonism + cerebellar signs
  • waning levodopa response
  • atypical dyskinesia
89
Q

what will a SPECT (DaT scan) show in Parkinson’s disease

A

decreased DA in basal ganglia

90
Q

1st line treatment for Parkinson’s disease if affecting function

A

co-beneledopa (levodopa + decarboxylase inhibitor)

91
Q

side effects of L-DOPA (DOPAMINE)

A
  • dyskinesia
  • on-off phenomena (motor fluctuations - freezing)
  • psychosis + psych symptoms - impulse control disorder
  • ABP decreased (postural hypotension)
  • mouth dryness
  • insomnia
  • N+V
  • EDS (excessive daytime sleepiness)
92
Q

what can happen if you stop L-DOPA suddenly

A

NMS!

pyrexia, muscle rigidity, HTN, tachycardia, tachypnoea, agitated delirium

93
Q

what is often raised in NMS

A

CK

AKI can develop secondary to rhabdomyolysis

94
Q

MRI findings in Huntington’s

A

atrophy of caudate nucleus + putamen

95
Q

downside of doing a non-contract CT head for stroke

A

normal in first few hours of ischaemic - but excludes haemorrhagic if normal

MRI higher sensitivity for infarct

96
Q

investigation to do for stroke if appropriate for thrombectomy

A

CT angiogram

97
Q

features of anterior cerebral artery stroke

A
  • contralateral hemiparesis
  • leg weakness > arm weakness
  • sparing of face
98
Q

features of middle cerebral artery stroke

A
  • arm weakness > leg weakness
  • contralateral hemiparesis
  • homonymous hemianopia (same side as paresis)
  • hemineglect if affecting non-dominant hemisphere
  • aphasia if affects dominant hemisphere (usually L)
  • UMN signs
99
Q

cause of lacunar syndrome

A

small perforating arteries being blocked i.e. internal capsule

100
Q

features of lacunar syndrome

A
  • ‘capsular warning syndrome’ = sudden onset weakness which relapses/remits
  • 1 of: pure hemimotor/hemisensory loss/pure sensorimotor loss/ataxic hemiparesis/contralateral lower face paralysis
101
Q

features of posterior cerebral artery stroke

A

contralateral homonymous hemianopia with macular sparing

contralateral loss of pain + temp

102
Q

what is Wallenberg’s syndrome

A

lateral medullary syndrome:

  • ipsilateral facial loss of pain + temp
  • ipsilateral Horner’s
  • ipsilateral cerebellar signs - ataxia
  • contralateral loss of pain + temp, limb sensory loss
103
Q

features of vertebral artery stroke

A
  • ipsilateral CN, contralateral long tract
  • bulbar dysfunction
  • ipsilateral cerebellar signs
  • nystagmus
104
Q

features of basilar artery occlusion (stroke)

A

locked in syndrome

105
Q

features of Weber’s (midbrain infarct)

A
  • oculomotor palsy (CNIII)
  • contralateral hemiplegia
  • can have Parkinsonian features
106
Q

causes of 1st order (central) Horner’s syndrome

A
  • MS
  • spondylosis
  • SOL
  • syringomyelia
  • stroke/lateral medullary syndrome (Wallenberg’s)
107
Q

causes of 2nd order (pre-ganglionic) Horner’s syndrome

A
  • pan coast tumour
  • cervical rib
  • thyroid carcinoma/goitre
108
Q

causes of 3rd order (post-ganglionic) Horner’s syndrome

A
  • carotid artery dissection

- radial neck dissection

109
Q

when can you do thrombolysis for stroke (alteplase)

A
  • <4.5 hour symptom onset

- must rule out haemorrhage first (CT)

110
Q

contraindications for thrombolysis for store

A
  • head trauma <3 months
  • > 180/>110 BP
  • anticoagulation (INR >1.7, DOAC within last 24 hours)
111
Q

when can you do thrombectomy for stroke

A

offer within 6h symptom onset with IV thrombolysis (if <4.5h) if occlusion of proximal anterior circulation (do CTA/MRA)

offer within 6-24h if above + potential to salvage brain tissue on CT

112
Q

antiplatelets to give after ischaemic stroke

A
  • aspirin 300mg once haemorrhage excluded for 2/52
  • clopidogrel after 2 week aspirin dose (MR dipyridamole if this is CI)

only give anticoagulation if in AF

113
Q

driving rules for CAR after stoke

A
  • don’t drive for a month (TIA or stroke)
  • don’t need to inform DVLA if no residual neurological deficit
  • multiple TIAs over a short period = no driving for 3 months
114
Q

driving rules for HEAVY GOODS VEHICLE after stroke

A

1 year after TIA/stroke

115
Q

when to do a CT in TIA

A

only if anticoagulated /haemoglobinopathy to exclude haemorrhage

116
Q

treatment of TIA

A
  • aspirin 300mg (+PPI)
  • refer to TIA clinic in 24h
  • statins
117
Q

when to do carotid endarterectomy for TIA

A

within 2 weeks if >70% stenosis and operative risk acceptable

118
Q

treatment of benign essential tremor

A

propranolol

119
Q

what to prescribe with analgesia for migraine

A

pro kinetic antiemetic e.g. metoclopramide

120
Q

where are the lewy bodies in LBD

A

LBs in occipito-parietal cortex

121
Q

what are Pick bodies

A

Tau protein (in Pick’s disease - type of front-temporal dementia)

122
Q

definition of a relapse in MS

A

new/worsening of pre-existing symptoms attributable to demyelinating disease lasting >24 hours in absence of infection or any cause - after stable period tf 1 month+

123
Q

typical demyelinating syndromes in MS

A
  • optic neuritis
  • transverse myelitis (SPASTIC PARAPERESIS)
  • cerebellar-related symptoms: ataxia, vertigo, clumsiness
  • brainstem syndromes: ataxia, eye movement abnormalities, bulbar muscle problems
124
Q

features of transverse myelitis

A
  • sensory and/or motor symptoms below level of inflammation
  • 2-3 vertebral segments
  • Lhermitte’s phenomena
  • trigeminal neuralgia
  • sphincter disturbance
125
Q

what is Lhermitte’s phenomena

A

neck flexion = electrical shocks in trunk/limbs

126
Q

approach to diagnosis of MS

A

2+ relapses:

  • objective clinical evidence of 2+ lesions OR
  • objective clinical evidence of 1 lesion with a reasonable history of a previous relapse

objective evidence = abnormality on neuro exam, MRI

127
Q

findings on LP of MS

A

oligoclonal bands found in CSD and NOT in serum

increased IgG

128
Q

findings indicating MS on MRI brain + spine with contrast

A
  • demyelinating plaques - periventricular plaques are called Dawson’s fingers + are found perpendicular to lateral ventricles
  • high signal T2 lesions in 2+ different CNS areas
129
Q

management of acute MS relapse

A

oral/IV methylprednisolone for 5 dyas

130
Q

disease modifying drugs for MS

A

beta interferon

131
Q

treatment of spasticity in MS

A

baclofen + gabapentin

132
Q

most common primary tumour of brain in adults

A

grade IV astrocytoma

133
Q

investigations to do for vesticular schwannoma/acoustic neuroma

A

gadolinium-enhanced MRI cerebellopontine angle + AUDIOMETRY

134
Q

bilateral acoustic neuromas are associated with

A

NF2

135
Q

myotomes for shoulder abduction and adduction

A
  • abduction = C5

- adduction = C5, C6

136
Q

myotomes for elbow flexion and extension

A
  • flexion = C5, C6

- extension = C7

137
Q

myotomes for wrist flexion and extension

A
  • flexion = C7, C8

- extension (and finger extension) = C7

138
Q

myotomes for finger flexion, abduction and adduction

A
  • flexion = C8

- abduction/adduction = T1

139
Q

myotomes for hip flexion and extension

A
  • flexion = L1, L2

- extension = L5, S1

140
Q

myotome for hip adduction

A

L2, L3

141
Q

myotomes for knee extension and flexion

A
  • extension = L3, L4

- flexion = L5, S1

142
Q

myotomes for ankle dorsiflexion and plantarflexion

A
  • dorsiflexion = L4, L5

- plantarflexion = S1

143
Q

which nerve root compressions have a positive femoral stretch test and weak quadriceps

A

L3 and L4

144
Q

which nerve root compressions have a positive sciatic nerve stretch test

A

L5 and S1

145
Q

cause of Brown-Sequard syndrome

A

spinal cord hemisection - due to trauma, radiation, haematoma, disc herniation, neoplasms

146
Q

features of Brown-Sequard syndrome

A
  • ipsilateral spastic paresis below lesion
  • ipsilateral loss of proprioception + vibration sense
  • contralateral loss of pain + temp sense below lesion
147
Q

additional symptom of progressive supra nuclear palsy (PSP) compared to Parkinson’s disease

A

same symptoms as PD

PLUS

vertical gaze palsy

148
Q

common neurological complication of diabetes

A

autonomic neuropathy - may present with postural hypotension and gastroparesis

149
Q

what is radiculopathy

A

pain in distribution of dermatome - caused by disease affecting root of spinal nerve

150
Q

cause of syringomyelia

A

collection of CSF within spinal cord due to e.g. chair malformation, trauma, SOL

can cause Horner’s if compresses sympathetic chain

151
Q

features of syringomyelia

A

‘cape-like’ loss of sensation to temperature and pain but preservation of light touch, proprioception and vibration

UMN signs if CST affected
LMN signs if anterior horn affected

152
Q

investigations for syringomyelia

A
  • full spine MRI to exclude tumour/tethered cord

- brain MRI to exclude chair malformation

153
Q

cause of SACDC

A

B12 deficiency = degeneration of dorsal + lateral CSTs + spinocerebellar tracts

154
Q

which reflexes are ABSENT in SACDC

A

ankle jerks absent - UMN signs typically in legs (extensor plantars, brisk knee reflexes, absent ankle jerks)

155
Q

location of damage in cauda equina

A

L1-L5

156
Q

1st line analgesia for back pain

A

NSAIDs

AVOID opiates

157
Q

causes of pinpoint pupils

A

opioids

brainstem haemorrhage

158
Q

normal ICP

A

7-15mmHg in adults in the supine position

159
Q

initial management of raised ICP

A
  • ABCDE
  • treat cause
  • elevate head to 30 degrees
  • IV mannitol
  • controlled hyperventilation to decrease CO2 (= vasoconstriction of cerebral arteries)
  • remove CSF e.g. drain from intraventricular monitor, repeated LP, ventriculoperitoneal shunt
160
Q

normal CSF opening pressure

A

12-18 mCSF

161
Q

investigation and management for hydrocephalus

A

MRI

do VP shunt

162
Q

visual findings in idiopathic intracranial hypertension

A

blurred vision
CNVI palsy
enlarged blind spot

163
Q

CN palsy in extradural haematoma

A

CNIII

164
Q

gold standard investigation for SAH

A

CT angiography

165
Q

management of SAD

A
  • nimodipine to prevent vasospasm

- endovascular coiling

166
Q

what is Terson’s syndrome

A

vitreous bleeds secondary to SAH

167
Q

LP finding in Listeria meningitis

A

clear CSF and high lymphocytes

whereas usually is turbid and high polymorphs

168
Q

guidelines for CT before LP in meningitis

A
  • focal neurological signs
  • papilloedema
  • GCS <=12
  • persistent seizures
169
Q

types of hallucinations you can get in HSV encephalitis (usually HSV2)

A

olfactory hallucinations

170
Q

LP findings in viral encephalitis

A

increased CSF protein
lymphocytes

do PCR

171
Q

treatment of viral encephalitis

A
  • acyclovir (empirical within 30 mins) - if HSV continue 14 days
  • HIV = HAART
  • CMV = ganciclovir
172
Q

Antibody screen for AI encephalitis

A

LGI1
NMDA R
CASPR2

173
Q

management of AI encephalitis

A

1st line = steroids + IV immunoglobulin

2nd line (if not responding within 2 weeks) = rituximab + cyclophosphamide (with 1st line therapy continued)

174
Q

pathogens causing brain abscess

A
  • strep viridians
  • toxoplasmosis
  • HIV
175
Q

predisposing factors for brain abscesses

A
  • infections (ear, sinus, dental)
  • skull fracture
  • congenital heart disease
  • endocarditis
  • immunosuppression
176
Q

infections which can cause peripheral neuropathy

A

leprosy
lyme disease
HIV
diphtheriae

177
Q

drugs/substances which can cause peripheral neuropathy

A 
alcohol
organophosphates
amiodarone
recreational drugs
chemotherapy
ISONIAZID
178
Q

how does Guillain-Barre (GBS) present

A

acute symmetrical ascending flaccid weakness/paralysis progressing over <14 days

proximal > distal muscles

starts in legs

LMN signs in lower limbs

back pain

paraesthesia in extremities

179
Q

cause of GBS

A

preceding illness i.e. campylobacter, CMV, mycoplasma 1-3 weeks before

180
Q

investigation findings in GBS

A
  • absent reflexes
  • nerve conduction studies = absent/prolonged f waves
  • CSF
  • ABG - T2RF
181
Q

CSF findings in GBS

A

raised protein

NORMAL WCC and glucose

182
Q

management of GBS

A
  • supportive (airway etc)
  • IV immunoglobulins, steroids exchange

NB: steroids don’t work

183
Q

CN signs in GBS

A
  • ophthalmoplegia diplopia
  • bilateral CNVII palsy
  • bulbar palsy
184
Q

what is Miller-Fisher syndrome

A

GBS variant - ataxia, ophthalmoplegia + areflexia

Year 5 notes (10 decks)

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